Left Ventricular (LV) Thrombus
- LV thrombus is usually seen in patients presenting with large anterior STEMI’s.
- Late presentation is an important risk factor
- LV thrombus results from the perfect storm of factors contributing to “Virchows Triad”:
- LV wall akinesis/dyskenia resulting in stagnant blood flow
- Pro-coagulative state
- Inflammation (due to ischemia)
- The incidence of LV thrombus is about 5-7% in anterior MI.
- (number may be smaller with modern reperfusion times)
- Imaging options:
- Echo (most commonly used)
- CT, or MRI.
- LV thrombus forms 12-72hrs after MI.
- Imaging too early in their MI course may not identify an LV thrombus
Treatment of LV Thrombus
- The most dreaded complication of LV thrombus is stroke.
- Vitamin K antagonists
- DOACs are available, but only used if VKA intolerant (no clinical trials available, case reports only)
- Primary Prevention in Anterior MI
- CCS 2018 – No routine anticoagulation (citing poor evidence and high risk of bleeding)
- AHA 2013 – Class IIB indication for anticoagulation
- Generally treat with anticoagulation for 3-6 months with a repeat echo to reassess that the LV thrombus has resolved.
|CCS 2018 Heart Failure Guidelines|
|AHA 2013 STEMI Guidelines|
Left Ventricular Aneurysm and Pseudoaneurysm
- Left ventricular aneurysm
- Result of thinning of the myocardium.
- Identified by a large neck.
- Low risk of rupture
- Persistent ST elevation on their EKG.
- Left ventricular pseudoaneurysm
- Cardiac myocardial rupture that is contained by the pericardium
- Very narrow neck
- High risk for rupture -> increased mortality
Right Ventricular (RV) Infarct
- Complication of inferior STEMI’s.
- No RV contractility to maintain forward flow, which leads to LV underfilling (reduced preload), reduced cardiac output, and hypotension.
- Drugs that further reduce preload such as nitrates and diuretics can worsen cardiac output leading to more hypotension and shock.
- RV is supplied mostly by the RV branch of the RCA. Proximal RCA lesion can compromise the RV branch.
- Important for early recognition and diagnosis of RV infarct.
EKG Findings in RV Infarct
- Indirect Evidence of RV Infarction:
- ST elevation in lead III > Lead II (Suggests RCA occlusion)
- ST elevation in V1 (Remember V1 is closest to the RV on a typical 12 lead EKG).
- ST elevation in V1 but ST depression in V2 -> suggestive of RV infarct.
- Direct Evidence of RV Infarction
- ST elevation in V4R (15 lead EKG is required). V4Reverse puts a lead directly over the RV.
- Remember only 0.5mm of ST elevation is required to be considered positive in V4R.
- RCA lesions are most common reason for RV infarct as the RV branch is supplied by the RCA.
- Usually very proximal lesions.
- Can be useful in assessing the severity of an RV infarct.
- Visual qualitative assessment.
- TAPSE (Tricuspid Annular Plane Systolic Excursion) has been a validated tool to assess RV function.
- Involves am M-mode at the base of the RV to assess tricuspid annular motion.
- Normal ≥ 1.7 cm.
- TAPSE has been validated as a predictor of heart failure and survival.
- Tissue Doppler
- Systolic excursion (S’) of < 9.5 cm/sec is suggestive of RV dysfunction.
RV Infarct on ECHO
- Even after revascularization, the right ventricle may take some time to recover.
- Hypotension Management
- The main hemodynamic problem resulting from an RV infarction is reduced LV preload, which causes reduced cardiac output/shock and hypotension.
- Avoid therapies that further reduce preload (nitrates, narcotics, propofol, etc.)
- Use therapies to improve preload (IV fluids, vasopressors)
- Improves RV stroke volume, and improves RV afterload by reducing pulmonary vascular resistance
- Ideally used after revascularization because inotropes can cause complications during acute MI (arrhythmias, increase in infarct size, etc.)
Inferior Infarct related heart block:
- Usually RCA, rarely can be circumflex.
- Heart block associated with high-vagal tone Bezold-Jarisch reflex or rarely from AV node ischemia
- Often transient and can be treated with atropine.
- Pacemaker should generally be avoided due to risk of RV perforation (can be placed in extreme circumstances)
Anterior Infarct related heart block:
- Usually related to extensive infarct and damage to the conduction system in the septum.
- Complete heart block often preceded by RBBB + LAFB.
- Temporary/permanent pacemaker more likely to be required usually see more distal conduction disease like Mobitz 2, third degree heart block, or alternating bundle branch blocks.
Ventricular Septal Defect
- A very uncommon complication of acute MI.
- Typically seen in late presenting patients who have not been revascularized. They are often female, older patients, and have no history of MI/Angina prior to presentation (less collaterals).
- Often have poor prognosis.
- Anterior Infarct often located at the apical ventricular septal.
- Inferior Infarct often located at the inferobasal ventricular septum. Usually a worse prognosis.
- Prominent pan-systolic murmur at left lower sternal border often associated with a thrill.
- Signs of right sided heart failure, pulmonary edema or shock.
- Echo helps confirm evidence of a VSD with left to right shunt as well as complications such as RV failure.
- Hemodynamic support with ionotropes, afterload reduction with nitroprusside and can consider IABP for mechanical support as bridge to surgery.
- Surgical closure or percutaneous options.
- Uncommon complication but very high mortality.
- The risk factors are similar to VSD’s. Patients are often older, late presenting, female, first presentation MI (lack of collaterals).
- Patients can have sudden PEA arrest from cardiac tamponade.
- Myocardial rupture is typically preceded by pain similar to the patients initial presentation.
- Hypertension, excessive straining, coughing, or vomiting may be triggers.
- Cardiac Arrest -> Standard ACLS plus pericardiocentesis.
- Hemodynamic compromise -> Fluids, dobutamine/pressors, pericardiocentesis.
- Traditionally there was concern regarding pericardiocentesis in that performing it would leave to clot dislogement and worsen leak. However, if there is hemodynamic compromise a pericardiocentesis should be performed, minimal fluid should be removed in order to restore hemodynamics (10-50ml).
- Surgical consultation is a must. Teflon or pericardial patch can be performed on the epicardium to stabilize the rupture.
Papillary Muscle Rupture
- Pulmonary edema
- Murmur may not be very loud (because of rapid equalization of pressures across the mitral valve) but patients will have severe MR.
- Posteromedial papillary muscle
- Most common
- Single blood supply PDA.
- Anterolateral papillary muscle
- Dual blood supply from the LAD and Circumflex.
- URGENT Surgical Consult
- Primary Author: Dr. Daniel Durocher (MD FRCPC)
- Dr. Pavel Antiperovitch (MD, FRCPC)